Proposal for the use of an inhalation drug containing 2-5 oligoadenylates for treatment of COVID-19

Bruchelt, Gernot; Treuner, J.; Schmidt, Karl‐Heinz

doi:10.1016/j.mehy.2022.110969

Cited by 1 publication

(1 citation statement)

References 33 publications

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“…In COVID-19, they are linked with the antiviral response and demonstrate consistent trends of enhanced inflammatory reactions in patients with severe COVID-19 (Gao et al 2021 ; Wang et al 2022 ; Alberts et al 2022 ; Guo et al 2022 ). The 2’-5’ oligoadenylate synthetase (OAS) gene family, including OAS1, OAS2, and OAS3, are closely related to the IFN-I/II-mediated signaling pathway in SLE (Gao et al 2020 ) and are also tightly linked with the inflammatory response and production of IFN-I/II in COVID-19 (Lee, et al 2023 ; Bruchelt et al 2022 ). They might also be essential mediators in concurrent heart failure and cardiac injury in patients with COVID-19 (Gao et al 2023 ).…”

Section: Discussionmentioning

confidence: 99%

Multi-omics analysis uncovered systemic lupus erythematosus and COVID-19 crosstalk

Nian,

Mao,

et al. 2024

Mol Med

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Background Studies have highlighted a possible crosstalk between the pathogeneses of COVID-19 and systemic lupus erythematosus (SLE); however, the interactive mechanisms remain unclear. We aimed to elucidate the impact of COVID-19 on SLE using clinical information and the underlying mechanisms of both diseases. Methods RNA-seq datasets were used to identify shared hub gene signatures between COVID-19 and SLE, while genome-wide association study datasets were used to delineate the interaction mechanisms of the key signaling pathways. Finally, single-cell RNA-seq datasets were used to determine the primary target cells expressing the shared hub genes and key signaling pathways. Results COVID-19 may affect patients with SLE through hematologic involvement and exacerbated inflammatory responses. We identified 14 shared hub genes between COVID-19 and SLE that were significantly associated with interferon (IFN)-I/II. We also screened and obtained four core transcription factors related to these hub genes, confirming the regulatory role of the IFN-I/II-mediated Janus kinase/signal transducers and activators of transcription (JAK-STAT) signaling pathway on these hub genes. Further, SLE and COVID-19 can interact via IFN-I/II and IFN-I/II receptors, promoting the levels of monokines, including interleukin (IL)-6/10, tumor necrosis factor-α, and IFN-γ, and elevating the incidence rate and risk of cytokine release syndrome. Therefore, in SLE and COVID-19, both hub genes and core TFs are enriched within monocytes/macrophages. Conclusions The interaction between SLE and COVID-19 promotes the activation of the IFN-I/II-triggered JAK-STAT signaling pathway in monocytes/macrophages. These findings provide a new direction and rationale for diagnosing and treating patients with SLE–COVID-19 comorbidity.

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